The mechanism of carcinogenic action of polycyclic aromatic hydrocarbons is being investigated through the use of metabolism binding and tumorigenicity studies. The results from our metabolism studies of benzo(a)pyrene (BP) and 7,12-dimethylbenz(a)anthracene (DMBA) in tumor sensitive and resistant mice as analyzed by HPLC and our tumorigenesis studies of various BP, dibenz(a,h)anthracene, DMBA, chrysene, 7-methyl-benz(a)anthracene and benzo(e)pyrene metabolites and derivatives suggest that diolepoxides in the "bay region" of these hydrocarbons are important in their tumorigenic activity. Our binding studies suggest that BP-diol-epoxide interacts to a greater extent and with some degree of specificity to the internucleosomal region of chromatin. Approximately 85% of the binding of BP-diol-epoxide to chromatin is to DNA with a high specific activity to G-C rich regions of DNA. Through the use of inhibitors of BP tumorigenicity, our data suggest that the interactions of BP-diol-epoxide to the exocyclic nitrogen of guanines are important adducts in the initiation of the carcinogenic process.